Yiqi Fumai lyophilized injection attenuates doxorubicin-induced cardiotoxicity, hepatotoxicity and nephrotoxicity in rats by inhibition of oxidative stress, inflammation and apoptosis.
Yue GuAichun JuBingjie JiangJingze ZhangShuli ManChangxiao LiuWenyuan GaoPublished in: RSC advances (2018)
Doxorubicin (DOX) is one of the most effective antineoplastic drugs, however, its organ toxicity inhibits the clinical utility. This study was aimed at investigating the protective effects of Yiqi Fumai lyophilized injection (YQFM) against DOX-induced tissue injury and exploring the mechanisms which mediated reactive oxygen species (ROS), inflammation and apoptosis. The experiment was as follows: rats were subjected to an intraperitoneal injection (i.p.) of YQFM (0.481 g kg -1 , i.p.) for 12 days; DOX (5 mg kg -1 , i.p.) was administered on the 4th, 8th and 12th days to achieve a cumulative dose of 15 mg kg -1 . Pretreatment of YQFM significantly ameliorated intracellular damage and dysfunction of the heart, liver and kidneys via decreasing activities of injury indexes. The levels of lipid peroxidation and glutathione depletion were clearly reduced following YQFM pretreatment, meanwhile the activities of glutathione peroxidase, superoxide dismutase, and catalase were elevated. Additionally administering YQFM could mitigate the cardiotoxicity, hepatotoxicity and nephrotoxicity via reducing levels of inflammatory factors and decreasing apoptosis. Accordingly, this study indicated that YQFM attenuated DOX-induced toxicity by ameliorating organ function, decreasing ROS production, and preventing excessive inflammation and apoptosis.
Keyphrases
- oxidative stress
- diabetic rats
- dna damage
- drug induced
- reactive oxygen species
- ischemia reperfusion injury
- induced apoptosis
- high glucose
- cell death
- cell cycle arrest
- endoplasmic reticulum stress
- drug delivery
- hydrogen peroxide
- ultrasound guided
- heat shock
- body mass index
- cell proliferation
- physical activity
- weight gain
- heat stress